Monlunabant is a selective CB1 antagonist that blocks CB1 receptor signaling to reduce appetite and fat accumulation, making it suitable for research on obesity and metabolic syndrome. Monlunabant binds to hCB1 and hCB2 with Ki values of 0.3 nM and 613 nM, respectively.

Monlunabant inhibits CB1-induced β-arrestin-2 recruitment (IC₅₀ = 21 pM) and G protein activation (IC₅₀ = 6 nM). [2]
Methods: INS-1 (832/13) rat insulinoma cells were incubated with Monlunabant (0.3, 3 nM) and glucose for 1 h, and insulin release was measured using AlphaLISA.
Results: Monlunabant significantly enhanced insulin secretion stimulated by 10 mM glucose at concentrations of 0.3 and 3 nM. [3]
Methods: Human islets (from 3 non-obese male donors with normal HbA1c levels) were treated with monlunabant (3 nM) and incubated for 30 min. After 30 min, treated with apoptotic cytokines (IL-1β (10 ng/mL) + IFNγ (100 ng/mL)), incubated for 48 h, and apoptosis and survival were assessed by flow cytometry (Annexin V-FITC / FVD eFlore 780).
Results: Monlunabant significantly reduced cytokine-induced apoptosis. [3]

Methods: Using CB1flox/flox mice as controls, a single oral dose of monlunabant (3 mg/kg) was administered. One and a half hours later, ethanol (5 g/kg) was administered orally, and the mice were sacrificed 3 hours after ethanol administration.
Results: Monlunabant significantly reduced alcohol-induced intestinal permeability in CB1flox/flox mice, upregulated tight junction protein mRNA, and decreased p-ERK1/2 expression. [1]
Methods: To investigate the effects of monlunabant on glucose metabolism, HFD-induced obese wild-type mice were administered a single oral dose of monlunabant (1 mg/kg). Clamping was initiated 1 hour after dosing, followed by detection of radiolabeled 2-deoxyglucose.
Results: Monlunabant increased systemic glucose clearance and enhanced 2-deoxyglucose uptake in skeletal muscle.[2]

DMSO: 80.00 mg/mL (135.36 mM), Sonication is recommended.